ArticleInflammation2024
Neutrophil Extracellular Traps Induce Pyroptosis of Rheumatoid Arthritis Fibroblast-Like Synoviocytes via the NF-κB/Caspase 3/GSDME Pathway.
Article in Inflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Acupuncture improves neurological function in ICH rats via suppression of WNK-SPAK-NKCC1 signaling activation.Journal of molecular histology · 2026Article
- Exploring the molecular mechanism of Er Miao San for treating rheumatoid arthritis based on network pharmacology.BMC complementary medicine and therapies · 2026Article
- Extracellular ATP induces the proinflammatory phenotype transition of MH7A cells by activating P2X7 receptor.Purinergic signalling · 2026Article
- Aquaporin-1 stabilizes β-catenin to promote NLRP3 inflammasome-mediated pyroptosis in rheumatoid arthritis.Apoptosis : an international journal on programmed cell death · 2026Article
- Cell-Free DNA-Based Theranostics for Inflammatory Disorders.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Activation of NF-κB signaling pathway in GSDME-low esophageal squamous cell carcinoma cells enhances radioresistance.Journal of translational medicine · 2026Article
- Catalpol mitigates rheumatoid arthritis by targeting neutrophil extracellular trap release.Frontiers in immunology · 2026Article
- AGTR1 inhibits pyroptosis and inflammatory cytokine secretion in rheumatoid arthritis fibroblast-like synoviocytes through the TGF-β pathway.American journal of translational research · 2026Article
- Neutrophil extracellular traps and pyroptosis: a molecular nexus linking systemic autoimmune diseases to atherosclerosis.Frontiers in immunology · 2026Review
- Neutrophil extracellular traps in diabetic wound healing: mechanisms, pathological roles, and therapeutic implications.Burns & trauma · 2026Review
- Frontier research on mechanisms of bone destruction in rheumatoid arthritis.Frontiers in cell and developmental biology · 2026Review
- The Application Prospects and Future Outlook ofDrug design, development and therapy · 2026Review
- RRM2 contributes to pathogenic phenotype of fibroblast-like synoviocytes by activating NF-κB signaling and inhibiting ferroptosis in rheumatoid arthritis.Journal of orthopaedic surgery and research · 2025Article
- Butin regulates the NLRP3/CASP-1/GSDMD pyroptosis axis to inhibit proliferation and pyroptosis in human fibroblast-like synoviocytes of rheumatoid arthritis.Scientific reports · 2025Article
- Cell death signaling and immune regulation: new perspectives on targeted therapy for sepsis.Cellular & molecular biology letters · 2025Review
- A new type of Caspase-1 upon recognizing bacteria inhibits GSDME-dependent histone modification and NF-κB signaling.Communications biology · 2025Article
- Neutrophils: a Central Point of Interaction Between Immune Cells and Nonimmune Cells in Rheumatoid Arthritis.Clinical reviews in allergy & immunology · 2025Review
- Biomaterials for Modulating the Immune Microenvironment in Rheumatoid Arthritis.BME frontiers · 2025Review
- The role of fibroblast-neutrophil crosstalk in the pathogenesis of inflammatory diseases: a multi-tissue perspective.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is an enduring, progressive autoimmune disorder. Abnormal activation of fibroblast-like synoviocytes (FLSs) has been proposed as the initiating factor for inflammation of the synovium and bone destruction. Neutrophil extracellular traps (NETs), which are web-like structures composed of DNA, histones, and granule proteins, are involved in the development of RA in multiple aspects. Pyroptosis, gasdermin-mediated inflammatory programmed cell death, plays a vital function in the etiopathogenesis of RA. However, the exact mechanism underlying NETs-induced pyroptosis in FLSs of RA and its impact on cellular pathogenic behavior remain undefined. In this study, we demonstrated that gasdermin E (GSDME) expression was upregulated in RA plasma and synoviums, which was positively correlated with the elevated cell-free DNA (cfDNA) and citrullinated histone 3 (Cit H3) levels in the plasma. Additionally, in vitro experiments have shown that NETs triggered caspase 3/GSDME-mediated pyroptosis in RA-FLSs, characterized by decreased cell viability, cell membrane blebbing, and rupture, as well as increased levels of pyroptosis-related proteins and pro-inflammatory cytokines. Again, silencing GSDME significantly inhibited pyroptosis and suppressed the migration, invasion, and secretion of pro-inflammatory cytokines in RA-FLSs. Furthermore, we also found that the nuclear factor-kappa B (NF-κB) pathway, serving as an upstream mechanism, was involved in FLS pyroptosis. In conclusion, our investigation indicated that NETs could induce RA-FLS pyroptosis and facilitate phenotypic transformation through targeting the NF-κB/caspase 3/GSDME axis. This is the first to explore the crucial role of NETs-induced FLS pyroptosis in the progression of RA, providing novel targets for the clinical management of refractory RA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.